This Month's CME

MANAGEMENT OF POISONING CASES AT GENERAL PRACTITIONER LEVEL

While practicing in rural area we have to counter poisoning cases many times. May it be accidental or suicidal timely & proper intervention can save many lives. For that we should know proper management of poisoning cases i.e. ABC OF POISIONING MANAGEMENT.

We should know the concept of TOXIDROMES, common procedures in poisoning management & DO'S & DO NOT'S at GP level.

in this article we will study detailed aspects of poisoning managagement. Let us first see/download the slide show

SHOCK:Dr.B.B.Sheikh,Nandurbar

SHOCK:Dr.B.B.Sheikh,Nandurbar

INTRODUCTION

Shock is a state of severe systemic reduction in tissue perfusion characterized by decreased cellular oxygen delivery and utilization as well as decreased removal of waste byproducts of metabolism. Hypotension, although common in shock, is not synonymous to shock. One can have hypotension and normal perfusion, or shock without hypotension in a patient who is usually very hypertensive. Shock is the final preterminal event in many diseases. Progressive tissue hypoxia results in loss of cellular membrane integrity, a reversion to a catabolic state of anaerobic metabolism, and a loss of energy-dependent ion pumps and chemical and electrical gradients. Mitochondrial energy production begins to fail. Multiple organ dysfunction follows localized cellular death, and organism death follows. Despite recent advances in treatment, mortality remains high: >60% in cardiogenic shock and >35% in septic shock

PATHOPHYSIOLOGY OF SHOCK

One method of evaluating shock is to recall the determinants of systemic blood pressure. Blood pressure is determined by the formula BP = systemic vascular resistance (SVR) × cardiac output (CO), where CO = heart rate (HR) × stroke volume (SV). SV = end diastolic volume (EDV)-end systolic volume (ESV). EDV is the filled ventricular volume prior to systolic contraction averaging about 100 cc in many adults. ESV is residual blood left in the ventricle after emptying during systole averaging about 40 cc. Therefore, the determinants of blood pressure are vascular resistance, HR, preload volume, and contractility (see Figure 9-1). SVR is the vascular "tone" and is a large determinant of diastolic blood pressure. EDV is largely determined by a preload volume that augments SV via Frank-Starling curves where increases in diastolic filling volumes increase CO. ESV is determined largely by cardiac contractility and it decreases as the heart ejects a greater percentage of its diastolic volume. For example, one can increase SV by increasing preload (EDV) with volume or decreasing ESV with increased contractility. The ejection fraction ((EDV - ESV)/EDV) thus increases

The initial derangement precipitating a state of shock might be (1) vasodilation (causing a decreased SVR) from sepsis, anaphylaxis, drugs, or cervical cord lesion, (2) extremes of HR, (3) loss of preload volume (causing decreased EDV) from blood or volume loss, or (4) loss of contractility (increasing the ESV) from heart failure. Compensatory mechanisms come into play and provide many of the clinical clues to early shock

volume loss increases, tachycardia and hypotension ensue. Loss of contractility also is compensated by increases in SVR to maintain blood pressure with similar symptoms

Once compensatory mechanisms fail, irreversible shock occurs with irreversible cell death, microcirculation plugging, and free radical generation. There is loss of autonomic regulation due to local nitric oxide vasodilator generation, and even with complete correction of blood volume (for example, in hypovolemic shock), tissue function and organ function are not restored, causing eventual death

CLASSIFICATION OF SHOCK

The major classical classification of shock includes (1) hypovolemic, (2)cardiogenic, (3)distributive, and (4)obstructive shock.